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    The endoplasmic reticulum–resident E3 ubiquitin ligase Hrd1 controls a critical checkpoint in B cell development in mice

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    J.Biol.Chem.-2018-Yang-12934-44.pdf
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    Final Published version
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    Author
    Yang, Yi
    Kong, Sinyi
    Zhang, Yana
    Melo-Cardenas, Johanna
    Gao, Beixue
    Zhang, Yusi
    Zhang, Donna D.
    Zhang, Bin
    Song, Jianxun
    Thorp, Edward
    Zhang, Kezhong
    Zhang, Jinping
    Fang, Deyu
    Show allShow less
    Affiliation
    Univ Arizona, Dept Pharmacol & Toxicol
    Issue Date
    2018-08-17
    Keywords
    lymphocyte
    unfolded protein response (UPR)
    ubiquitin ligase
    ubiquitin
    protein turnover
    pre-BCR
    
    Metadata
    Show full item record
    Publisher
    AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
    Citation
    Yang, Yi & Kong, Sinyi & Zhang, Yana & Melo-Cardenas, Johanna & Gao, Beixue & Zhang, Yusi & D. Zhang, Donna & Zhang, Bin & Song, Jianxun & Thorp, Edward & Zhang, Kezhong & Zhang, Jinping & Fang, Deyu. (2018). The endoplasmic reticulum-–resident E3 ubiquitin ligase Hrd1 controls a critical checkpoint in B- cell development in mice. Journal of Biological Chemistry. 293. jbc.RA117.001267. 10.1074/jbc.RA117.001267.
    Journal
    JOURNAL OF BIOLOGICAL CHEMISTRY
    Rights
    © 2018 by The American Society for Biochemistry and Molecular Biology, Inc.
    Collection Information
    This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.
    Abstract
    Humoral immunity involves multiple checkpoints that occur in B cell development, maturation, and activation. The pre-B-cell receptor (pre-BCR) is expressed following the productive recombination of the immunoglobulin heavy-chain gene, and sSignalsing through the pre-BCR are required for the differentiation of pre-B cells into immature B cells. However, the molecular mechanisms controlling the pre-BCR expression and signaling strength remain undefined. Herein, we probed the role of the endoplasmic reticulum-associated, stress-activated E3 ubiquitin ligase HMG-CoA reductase degradation 1 (Hrd1) in B cell differentiation. Using mice with a specific Hrd1 deletion in pro-B cells and subsequent B cell developmental stages, we showed that the E3 ubiquitin ligase Hrd1 governs a critical checkpoint during B cell development. We observed that Hrd1 is required for degradation of the pre-BCR complex during the early stage of B cell development. As a consequence, loss of Hrd1 in the B cell lineage resulted in increased pre-BCR expression levels and a developmental defect in the transition from large to small pre-B cells. This defect, in turn, resulted in reduced fewer mature B cells in bone marrow and peripheral lymphoid organs. Our results revealed a novel critical role of Hrd1 in controlling a critical checkpoint in B cell-mediated immunity and suggest that Hrd1 may functioning as an E3 ubiquitin ligase of the pre-BCR complex.
    Note
    12 month embargo; published online: 15 June 2018
    ISSN
    0021-9258
    1083-351X
    PubMed ID
    29907570
    DOI
    10.1074/jbc.RA117.001267
    Version
    Final published version
    Sponsors
    National Institutes of Health [AI079056, AI108634, AR006634]; National Natural Science Foundation of China (NSFC) [81600784, 31270939, 81471526, 81771667]; Training Program of the Major Research Plan in regional immunology of the National Natural Science Foundation of China [91442110]; Natural Science Foundation of Jiangsu Province [BK20170349]; postdoctoral foundation of China; Social development project of Jiangsu Province Grant [BE2016676]; Jiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences of Soochow University
    Additional Links
    http://www.jbc.org/lookup/doi/10.1074/jbc.RA117.001267
    ae974a485f413a2113503eed53cd6c53
    10.1074/jbc.RA117.001267
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